Discovery of recurrent t(6;7)(p25.3;q32.3) translocations in ALK-negative anaplastic large cell lymphomas by massively parallel genomic sequencing
Makaleler > Tam Makale · 2010
Yazarlar: Andrew L. Feldman, Ahmet DOGAN, David I. Smith, Mark E. Law, Stephen M. Ansell, Sarah H. Johnson, Julie C. Porcher, Nazan ÖZSAN, Eric D. Wieben, Bruce W. Eckloff, George VASMATZİS
Blood, SCI Expanded İndekslerine Giren Dergi, Uluslararası, Wos, 2010, cilt 117, ss 915-919
DOI: 10.1182/blood-2010-08-303305
Özet
The genetics of peripheral T-cell lymphomas are poorly understood. The most well-characterized abnormalities are translocations involving ALK, occurring in approximately half of anaplastic large cell lymphomas (ALCLs). To gain insight into the genetics of ALCLs lacking ALK translocations, we combined mate-pair DNA library construction, massively parallel ("Next Generation") sequencing, and a novel bioinformatic algorithm. We identified a balanced translocation disrupting the DUSP22 phosphatase gene on 6p25.3 and adjoining the FRA7H fragile site on 7q32.3 in a systemic ALK-negative ALCL. Using fluorescence in situ hybridization, we demonstrated that the t(6;7)(p25.3;q32.3) was recurrent in ALK-negative ALCLs. Furthermore, t(6;7)(p25.3;q32.3) was associated with down-regulation of DUSP22 and up-regulation of MIR29 microRNAs on 7q32.3. These findings represent the first recurrent translocation reported in ALK-negative ALCL and highlight the utility of massively parallel genomic sequencing to discover novel translocations in lymphoma and other cancers.